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The collection of spatialised electricity consumption data is considered of crucial importance for planning electric power facilities and achieving the United Nations Sustainable Development Goal 7 (SDG7). However, the predominance of statistical data on electricity consumption in China in combination with the lack of spatialised electricity consumption data for the past five years poses a serious challenge. To effectively address this issue, a nighttime light remote sensing estimation model of China’s electricity consumption was developed in this work. Specifically, NPP-VIIRS nighttime light and publicly available electricity consumption data were used, and a spatialised Chinese electricity consumption data product for the period 2012–2023 was derived. At the same time, the time–space variation of China’s electricity consumption was systematically analysed. For the spatial dimension, the power function model was proven to be the most suitable estimation model for China, with an average R2 of 0.9385, while for the temporal dimension, the quadratic polynomial model was the most suitable, with an R2 of 0.9706. From the analysis of time–space variation, an increase in both the number and extent of high electricity consumption areas was observed, particularly in third- and fourth-tier cities in the south, while some industrial cities experienced a decline in electricity consumption.

Canonical WNT signaling is required for proper vascularization of the CNS during embryonic development. Here, we used mice with targeted mutations in genes encoding canonical WNT pathway members to evaluate the exact contribution of these components in CNS vascular development and in specification of the blood-brain barrier (BBB) and blood-retina barrier (BRB). We determined that vasculature in various CNS regions is differentially sensitive to perturbations in canonical WNT signaling. The closely related WNT signaling coreceptors LDL receptor-related protein 5 (LRP5) and LRP6 had redundant functions in brain vascular development and barrier maintenance; however, loss of LRP5 alone dramatically altered development of the retinal vasculature. The BBB in the cerebellum and pons/interpeduncular nuclei was highly sensitive to decrements in canonical WNT signaling, and WNT signaling was required to maintain plasticity of barrier properties in mature CNS vasculature. Brain and retinal vascular defects resulting from ablation of Norrin/Frizzled4 signaling were ameliorated by stabilizing β-catenin, while inhibition of β-catenin-dependent transcription recapitulated the vascular development and barrier defects associated with loss of receptor, coreceptor, or ligand, indicating that Norrin/Frizzled4 signaling acts predominantly through β-catenin-dependent transcriptional regulation. Together, these data strongly support a model in which identical or nearly identical canonical WNT signaling mechanisms mediate neural tube and retinal vascularization and maintain the BBB and BRB.

The brain, spinal cord, and retina are supplied by capillaries that do not permit free diffusion of molecules between serum and parenchyma, a property that defines the blood-brain and blood-retina barriers. Exceptions to this pattern are found in circumventricular organs (CVOs), small midline brain structures that are supplied by high permeability capillaries. In the eye and brain, high permeability capillaries are also present in the choriocapillaris, which supplies the retinal pigment epithelium and photoreceptors, and the ciliary body and choroid plexus, the sources of aqueous humor and cerebrospinal fluid, respectively. We show here that (1) endothelial cells in these high permeability vascular systems have very low beta-catenin signaling compared to barrier-competent endothelial cells, and (2) elevating beta-catenin signaling leads to a partial conversion of permeable endothelial cells to a barrier-type state. In one CVO, the area postrema, high permeability is maintained, in part, by local production of Wnt inhibitory factor-1.

As a chronic illness derived from hair cells of the inner ear, Menière's disease (MD) negatively influences the quality of life of individuals and leads to a number of symptoms, such as dizziness, temporary hearing loss, and tinnitus. The complete identification of novel genes related to MD would help elucidate its underlying pathological mechanisms and improve its diagnosis and treatment. In this study, a network-based method was developed to identify novel MD-related genes based on known MD-related genes. A human protein-protein interaction (PPI) network was constructed using the PPI information reported in the STRING database. A classic ranking algorithm, the random walk with restart (RWR) algorithm, was employed to search for novel genes using known genes as seed nodes. To make the identified genes more reliable, a series of screening tests, including a permutation test, an interaction test and an enrichment test, were designed to select essential genes from those obtained by the RWR algorithm. As a result, several inferred genes, such as CD4, NOTCH2 and IL6, were discovered. Finally, a detailed biological analysis was performed on fifteen of the important inferred genes, which indicated their strong associations with MD.

ObjectivesTo investigate the repeatability, reproducibility, and staging and monitoring of the performance of native T1 mapping for noninvasively assessing liver fibrosis in comparison with acoustic radiation force impulse (ARFI) elastography.MethodsThe repeatability and reproducibility were explored in 8 male Sprague-Dawley rats with intraclass correlation coefficient (ICC). Different degrees of fibrosis were induced in 52 rats by carbon-tetrachloride (CCl4) insult. Another 16 rats were used to build fibrosis progression and regression models. The native T1 values and shear wave velocity (SWV) were quantified by using native T1 mapping and ARFI elastography, respectively. The METAVIR system (F0–F4) was used for the staging of fibrosis. The area under the receiver operating characteristic curve (AUC) was determined to assess the performance of quantitative parameters for staging and monitoring fibrosis.ResultsNative T1 values shared similar good repeatability (ICC = 0.93) and reproducibility (ICC = 0.87) with SWV (ICC = 0.84–0.93). The AUC of native T1 values were 0.84, 0.84, and 0.75 for diagnosing significant fibrosis (≥ F2) and liver cirrhosis (F4) and detecting fibrosis progression, and those of SWV were 0.81, 0.86, and 0.7, respectively. No significant difference in performance was found between the two quantitative parameters (p ≥ 0.496). For detecting fibrosis regression, native T1 values had a better accuracy (AUC = 0.99) than SWV (AUC = 0.56; p = 0.002).ConclusionNative T1 mapping may be a reliable and accurate method for noninvasively assessing liver fibrosis. Compared with ARFI elastography, it provides similar good repeatability and reproducibility, a similar high accuracy for staging fibrosis, and a better accuracy for detecting fibrosis regression.Key Points• Native T1 mapping is a valuable tool for noninvasively assessing liver fibrosis and can be measured on virtually all clinical MRI machines without additional hardware or gadolinium chelate injection.• Compared with acoustic radiation force impulse elastography, native T1 mapping yields similar good repeatability and reproducibility and a similar high accuracy for staging fibrosis.• Native T1 mapping provides a significantly better performance for detecting fibrosis regression than acoustic radiation force impulse elastography.

In mice, postnatal endothelial cell (EC)-specific knockout of the genes coding for transforming growth factor-beta receptor (TGFBR)1 and/or TGFBR2 eliminates TGF-beta signaling in vascular ECs and leads to distinctive central nervous system (CNS) vascular phenotypes. Knockout mice exhibit (1) reduced intraretinal vascularization, (2) choroidal neovascularization with occasional anastomoses connecting choroidal and intraretinal vasculatures, (3) infiltration of diverse immune cells into the retina, including macrophages, T-cells, B-cells, NK cells, and dendritic cells, (4) a close physical association between immune cells and retinal vasculature, (5) a pro-inflammatory transcriptional state in CNS ECs, with increased ICAM1 immunoreactivity, and (6) increased smooth muscle actin immunostaining in CNS pericytes. Comparisons of the retinal phenotype with two other genetic models of retinal hypovascularization – loss of Norrin/Fzd4 signaling and loss of vascular endothelial growth factor (VEGF) signaling – show that the immune cell infiltrate is greatest with loss of TGF-beta signaling, more modest with loss of Norrin/Fzd4 signaling, and undetectable with loss of VEGF signaling. The phenotypes caused by loss of TGF-beta signaling in ECs recapitulate some of the cardinal features of retinal and neurologic diseases associated with vascular inflammation. These observations suggest that therapies that promote TGF-beta-dependent anti-inflammatory responses in ECs could represent a promising strategy for disease modulation.

The molecular basis of Wnt-Frizzled specificity is a central question in developmental biology. Reck, a multi-domain and multi-functional glycosylphosphatidylinositol-anchored protein, specifically enhances beta-catenin signaling by Wnt7a and Wnt7b in cooperation with the 7-transmembrane protein Gpr124. Among amino acids that distinguish Wnt7a and Wnt7b from other Wnts, two clusters are essential for signaling in a Reck- and Gpr124-dependent manner. Both clusters are far from the site of Frizzled binding: one resides at the amino terminus and the second resides in a protruding loop. Within Reck, the fourth of five tandem repeats of an unusual domain with six-cysteines (the CC domain) is essential for Wnt7a stimulation: substitutions P256A and W261A in CC4 eliminate this activity without changing protein abundance or surface localization. Mouse embryos carrying ReckP256A,W261A have severe defects in forebrain angiogenesis, providing the strongest evidence to date that Reck promotes CNS angiogenesis by specifically stimulating Wnt7a and Wnt7b signaling.

Based on the spread of COVID-19, in the present paper, an imperfectly vaccinated SVEIR model for latent age is proposed. At first, the equilibrium points and the basic reproduction number of the model are calculated. Then, we discuss the asymptotic smoothness and uniform persistence of the semiflow generated by the solutions of the system and the existence of an attractor. Moreover, LaSalle’s invariance principle and Volterra type Lyapunov functions are used to prove the global asymptotic stability of both the disease-free equilibrium and the endemic equilibrium of the model. The conclusion is that if the basic reproduction number Rρ is less than one, the disease will gradually disappear. However, if the number is greater than one, the disease will become endemic and persist. In addition, numerical simulations are also carried out to verify the result. Finally, suggestions are made on the measures to control the ongoing transmission of COVID-19.

Pod number is an important factor that influences yield in soybean. Here, we used two associated recombinant inbred line (RIL) soybean populations, RIL3613 (containing 134 lines derived from Dongnong L13 × Heihe 36) and RIL6013 (composed of 156 individuals from Dongnong L13 × Henong 60), to identify quantitative trait loci (QTLs) regulating the vertical distribution and quantity of seeds and seed pods. The numbers of pods were quantified in the upper, middle, and lower sections of the plant, as well as in the plants as a whole, and QTLs regulating these spatial traits were mapped using an inclusive complete interval mapping method. A total of 21 and 26 QTLs controlling pod-number-related traits were detected in RIL3613 and RIL6013, respectively, which explained 1.25-11.6698% and 0.0001-7.91% of the phenotypic variation. A total of 34 QTLs were verified by comparison with previous research, were identified in both populations, or were found to regulate multiple traits, indicating their authenticity. These results enhance our understanding of the vertical distribution of pod-number-related traits and support molecular breeding for seed yield.

Background Targeting tumor metabolism reprogramming has demonstrated a synergistic antitumor effect in photodynamic therapy of triple-negative breast cancer (TNBC). However, such a combination therapeutic regimen has encountered challenges, such as limited photosensitizer bioavailability and severe drug toxicity. Methods and results Herein, ultrasmall metal-organic frameworks (MOFs) nanodots (MSPC) that encapsulate metabolism inhibitors and mitochondria-targeted photosensitizers are designed and fabricated for synergistic photodynamic therapy (PDT) of TNBC. The MSPC exhibits an acidic-sensitive drug release, leading to glutathione depletion and mitochondrial respiration suppression. Significantly, MSPC substantially reduces intracellular adenosine triphosphate (ATP) levels by simultaneously disrupting oxidative phosphorylation and impeding aerobic glycolysis. Therefore, the glutathione depletion combined with metabolism inhibitor increases oxidative stress, which improves the efficacy of mitochondria-targeted PDT. Additionally, the increased retention of photosensitizers within tumors, facilitated by aggregation-enhanced retention (AER) effect, extends the time window for long-term fluorescence/photoacoustic imaging-guided PDT of TNBC. MSPC-sensitized PDT significantly suppresses tumor growth with a single-dose injection and repeatable PDT. Conclusions In summary, these renal-clearable and aggregation-enhanced tumor-retained nanodots indicate the feasibility of overcoming resistance to reactive oxygen species induced by metabolic reprogramming, thus holding significant implications for boosting PDT of TNBC. Graphical Abstract